Molecular basis of viral persistence: a single amino acid change in the glycoprotein of lymphocytic choriomeningitis virus is associated with suppression of the antiviral cytotoxic T-lymphocyte response and establishment of persistence.
about
The role of viral persistence in flavivirus biologyHepatitis C virus (HCV) circulates as a population of different but closely related genomes: quasispecies nature of HCV genome distributionInterleukin-10 determines viral clearance or persistence in vivoA live attenuated vaccine for Lassa fever made by reassortment of Lassa and Mopeia viruses.Type I interferon is a therapeutic target for virus-induced lethal vascular damage.Pathogenicity of Hantaan virus in newborn mice: genetic reassortant study demonstrating that a single amino acid change in glycoprotein G1 is related to virulenceTCR stimulation strength is inversely associated with establishment of functional brain-resident memory CD8 T cells during persistent viral infection.Inhibition of cellular entry of lymphocytic choriomeningitis virus by amphipathic DNA polymersTreatment with a sphingosine analog does not alter the outcome of a persistent virus infection.Differences in affinity of binding of lymphocytic choriomeningitis virus strains to the cellular receptor alpha-dystroglycan correlate with viral tropism and disease kinetics.Persistent virus infection inhibits type I interferon production by plasmacytoid dendritic cells to facilitate opportunistic infections.Augmented replicative capacity of the boosting antigen improves the protective efficacy of heterologous prime-boost vaccine regimens.Intrinsic functional dysregulation of CD4 T cells occurs rapidly following persistent viral infectionEvolution of recombinant lymphocytic choriomeningitis virus/Lassa virus in vivo highlights the importance of the GPC cytosolic tail in viral fitness.RING finger Z protein of lymphocytic choriomeningitis virus (LCMV) inhibits transcription and RNA replication of an LCMV S-segment minigenome.Posttranslational modification of alpha-dystroglycan, the cellular receptor for arenaviruses, by the glycosyltransferase LARGE is critical for virus binding.Minimal effect of CD103 expression on the control of a chronic antiviral immune response.Molecular indetermination in the transition to error catastrophe: systematic elimination of lymphocytic choriomeningitis virus through mutagenesis does not correlate linearly with large increases in mutant spectrum complexity.Effects of promyelocytic leukemia protein on virus-host balance.LCMV glycosylation modulates viral fitness and cell tropism.Recovery of an arenavirus entirely from RNA polymerase I/II-driven cDNAPoint mutation in the glycoprotein of lymphocytic choriomeningitis virus is necessary for receptor binding, dendritic cell infection, and long-term persistence.Reverse genetics approaches to combat pathogenic arenavirusesReprogramming of antiviral T cells prevents inactivation and restores T cell activity during persistent viral infectionDecoding arenavirus pathogenesis: essential roles for alpha-dystroglycan-virus interactions and the immune response.The role of dendritic cells in viral persistenceArenavirus variations due to host-specific adaptation.Pseudotyping lentiviral vectors with lymphocytic choriomeningitis virus glycoproteins for transduction of dendritic cells and in vivo immunization.Early virus-host interactions dictate the course of a persistent infectionLymphocytic choriomeningitis virus persistence promotes effector-like memory differentiation and enhances mucosal T cell distributionOpposing effects of CD70 costimulation during acute and chronic lymphocytic choriomeningitis virus infection of miceDirect infection of dendritic cells during chronic viral infection suppresses antiviral T cell proliferation and induces IL-10 expression in CD4 T cells.Infection of dendritic cells by lymphocytic choriomeningitis virus.Modulation of SIV and HIV DNA vaccine immunity by Fas-FasL signalingDevelopment of live-attenuated arenavirus vaccines based on codon deoptimizationInflammatory monocytes recruited to the liver within 24 hours after virus-induced inflammation resemble Kupffer cells but are functionally distinct.Loss of the signaling adaptor TRAF1 causes CD8+ T cell dysregulation during human and murine chronic infectionNatural killer cell activation enhances immune pathology and promotes chronic infection by limiting CD8+ T-cell immunityPolymicrobial Sepsis Increases Susceptibility to Chronic Viral Infection and Exacerbates CD8+ T Cell Exhaustion.Virus-induced immunosuppression: immune system-mediated destruction of virus-infected dendritic cells results in generalized immune suppression.
P2860
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P2860
Molecular basis of viral persistence: a single amino acid change in the glycoprotein of lymphocytic choriomeningitis virus is associated with suppression of the antiviral cytotoxic T-lymphocyte response and establishment of persistence.
description
1991 nî lūn-bûn
@nan
1991年の論文
@ja
1991年論文
@yue
1991年論文
@zh-hant
1991年論文
@zh-hk
1991年論文
@zh-mo
1991年論文
@zh-tw
1991年论文
@wuu
1991年论文
@zh
1991年论文
@zh-cn
name
Molecular basis of viral persi ...... establishment of persistence.
@ast
Molecular basis of viral persi ...... establishment of persistence.
@en
type
label
Molecular basis of viral persi ...... establishment of persistence.
@ast
Molecular basis of viral persi ...... establishment of persistence.
@en
prefLabel
Molecular basis of viral persi ...... establishment of persistence.
@ast
Molecular basis of viral persi ...... establishment of persistence.
@en
P2093
P2860
P921
P1433
P1476
Molecular basis of viral persi ...... d establishment of persistence
@en
P2093
E Shimomaye
M B Oldstone
P2860
P304
P407
P577
1991-04-01T00:00:00Z